We propose to further investigate the regulation of mitogen-induced T cell colony (TCC) growth in humans. The surface markers of the clonogenic cells derived from E-rosette positive and negative fractions will be determined. These markers include T-cell antigens Ia, Fc[unreadable]gamma[unreadable], Fc[unreadable]mu[unreadable], and complement receptors. The surface markers of the clonogenic cells from different tissues (nodes, blood, and marrow) and different cell fractions from these tissues will also be determined and compared. Next, a similar thorough analysis of the surface markers of both individual, expanded, and pooled colonies will be performed to determine if either colonies or whole cultures have single or multiple markers. The humoral and cellular regulation of TCC growth in our system will be further investigated for the following reasons: (1) to insure greater reproducibility; (2) to understand abnormalities in proliferation; and (3) to identify lymphoid cell fractions most ideal to create human T-cell hybridomas from. Some emphasis will be placed in B-T cell interactions in the production of TCC growth factors. In a further attempt to improve the assay human T-cell hybridomas will be screened for growth promoting activity in this system. It will also be determined if hybridomas secreting colony growth factors also secrete intraleukin II. In non-T human hematopoietic malignancies we will determine the frequency of TCC growth from a number of sites (marrow, blood, and nodes), and determine possible malignant origin by examining TCCs for nucleolar antigen and cytogenetic abnormalities. We will also determine the surface markers of the colony forming cells and colonies in these conditions and if they differ from normals. Finally, the clinical significance of TCC growth with abnormal markers will be evaluated. In chronic myeloid leukemia abnormal T-cell clones found by us in the benign phase of the disease will be expanded and their clonality and biological properties examined. It will be determined for myeloid leukemia and lymphoma if the presence of abnormal TCC growth is associated with a poorer response to therapy, shorter remission duration, and, if these abnormalities persist during remission, the relevance of this to remission duration. (LB)